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Blood, 15 November 2005, Vol. 106, No. 10, pp. 3432-3439.
Prepublished online as a Blood First Edition Paper on July 12, 2005; DOI 10.1182/blood-2005-04-1393.
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IMMUNOBIOLOGY
T-bet is required for optimal proinflammatory CD4+ T-cell trafficking
Graham M. Lord,
Ravi M. Rao,
Hyeryun Choe,
Brandon M. Sullivan,
Andrew H. Lichtman,
F. William Luscinskas, and
Laurie H. Glimcher
From the Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA; Eric Bywaters Centre for Vascular Inflammation, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom; the Department of Medicine and Children's Hospital, Department of Pediatrics, Harvard Medical School, Boston, MA; the Division of Infectious Diseases, University of California, San Francisco, San Francisco, CA; and the Vascular Research Division, Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital, Boston, MA.
Inflammatory responses are controlled by T helper 1 (Th1) lymphocytes. An important function of this polarity is the ability of T cells to traffick appropriately in vivo. This differential trafficking is dependent upon the binding of P-selectin glycoprotein ligand-1 to P- and E-selectin on inflamed endothelium as well as the expression of specific chemokine receptors. Here we show that in the absence of T-box expressed in T cells (T-bet), selective migration of T cells in vivo is completely abrogated and that T-bet regulates the binding of CD4+ T cells to P-selectin. T-bet is also required for the expression of the chemokine receptor CXCR3. Thus, T-bet controls Th1-cell migration to inflammatory sites, which has fundamental consequences for the control of immunologic disease.
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